Updated project metadata. Loss of BCL11B in human peripheral blood CD8+ T cells led to acquisition of an innate-like phenotype and the ability to efficiently lyse tumor cells either spontaneously via the NKp30/B7H6 axis or mediated by a GD2 antibody. The phenotype of BCL11B knock-out cells was investigated by characterization of surface marker profile, transcriptome, and proteome compared to control cells.